| Autor: |
Shibata, Yujiro, Takaoka, Masanori, Maekawa, Daisuke, Kuwahara, Chika, Matsumura, Yasuo |
| Zdroj: |
Journal of Cardiovascular Pharmacology; November 2004, Vol. 44 Issue: Supplement 1 pS459-S461, 3p |
| Abstrakt: |
It is known that 17β-estradiol (E2-β) increases the production of nitric oxide. We have demonstrated that E2-β prevents renal injury and suppresses renal endothelin-1 overproduction in ischemic acute renal failure in rats. In the present study, we investigated whether NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, can reverse the effect of E2-β in ischemic acute renal failure. Ischemic acute renal failure was induced by clamping the left renal artery and vein for 45 minutes followed by reperfusion, 2 weeks after contralateral nephrectomy. Pre-ischemic treatment with E2-β (100 μg/kg, intravenously) attenuated the ischemia/ reperfusion-induced renal dysfunction and suppressed the increment of renal endothelin-1 content 24 hours after reperfusion. The effects of E2-β on renal dysfunction and increased endothelin-1 content in acute renal failure rats were reversed by pretreatment with NG-nitro-L-arginine methyl ester (0.3 mg/kg, intravenously). An in vivo microdialysis study revealed that the concentration of nitric oxide metabolites in the kidney was reduced during ischemia, and quickly recovered after reperfusion in E2-β-treated acute renal failure rats, compared with cases in untreated acute renal failure rats. This recovery of renal nitric oxide metabolite concentration with E2-β was abolished by the pretreatment with NG-nitro-Larginine methyl ester. These findings suggest that nitric oxide is closely related to suppressive effect of E2-β on renal endothelin-1 overproduction in acute renal failure rats and this suppression is probably involved in the beneficial effect of E2-β on ischemia/reperfusion-induced renal injury. |
| Databáze: |
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